Undoubtedly lipidomics has allowed tremendous advances in understanding and determining the true importance of lipids and FAs in many physiological and molecular mechanisms implicated in the establishment of healthy or diseased status.
There is strong evidence that many of the pathogenic mechanisms implicated in acute neurodegenerative diseases, such as oxidative stress and inflammation, are equally involved in the slower neuronal loss characteristic of chronic neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), various tauopathies, and Huntington's disease (HD).
Many studies have aimed at dissecting mechanisms implicated in the disease, and it is now well accepted that injuries in ICU patients lead not only to the initiation of an uncontrolled and exacerbated pro-inflammatory response but also to a deep activation of anti-inflammatory processes [4].
There are two mechanisms implicated in the generation of pneumocephalus, "ball valve" and "inverted bottle".
Cell death, aberrant synaptogenesis, and synaptic plasticity and neuroinflammation constitute three key mechanisms implicated in epileptogenesis.
Figure 1 Principal mechanisms implicated in the development of microcirculatory alterations.
However, the mechanisms implicated are far from being clarified.
A recent hypothesis pointed out a possible role of oxidative stress as a key player in the pathogenesis of insulin resistance, cell dysfunction, and hypertension [ 46, 47] and many mechanisms have been implicated in processes underlying oxidative stress-mediated hypertension.
A vast literature implicates many mechanisms, including aberrations not only of ERα itself, but alterations in other molecules and signaling pathways consistent with heightened growth factor activity [ 76- 78].
Another important mechanism implicated in hematotoxicity and genotoxicity is programmed cell death (apoptosis).
